Gastrointestinal: MRCEM Primary questions with answers

Gastrointestinal physiology explains how food is moved, broken down and absorbed. It forms part of the physiology section of MRCEM Primary, which carries 60 of the 180 questions. The topic covers innervation and hormones, swallowing, saliva, the stomach, liver, bile, exocrine pancreas and small intestine, absorption of carbohydrates, proteins, lipids, iron, calcium and vitamins, and the large intestine. It helps explain vomiting, diarrhoea and liver disease in the emergency department.

5 free questions below, each with the answer and the full explanation · 161 in the full bank · Last updated after the 27 October 2026 MRCEM Primary sitting.

1. Question 1 · Calcium Absorption

   Which of the following diets is a rich source of calcium?

   1. ASun flower
   2. BBroccoli
   3. CSoyabean
   4. DTomato
   5. EBroccoli
   Show answer and explanation

   Answer: C. RCEM key: soyabean is a rich source of calcium.

   • A: Not the keyed rich calcium source.
   • B: Contains some calcium but less than the keyed soyabean.
   • D: Tomato is a low-calcium food.
   • E: Contains some calcium but less than the keyed soyabean.

   Full explanation

   Rcem key:  soyabean is a rich source of calcium

   Note: Dairy products which include cheese, leafy vegetables, and Soybean is rich in calcium.

   • Almond is also rich in calcium but if both almond and cheese are in option choose dairy product cheese because cheese has more calcium than almond per 100gm.

2. Question 2 · Summary of Hormones and Secretion of Git

   Vibrio cholera causes watery diarrhea through which of following final pathways?

   1. AIncrease proton secretory channels
   2. BIncreased hco3 secretory channels
   3. CDecrease Camp
   4. DDecreased cl- ion secretion
   5. EIncrease cl- ion secretion
   Show answer and explanation

   Answer: E. Raised cAMP activates Cl- secretory channels, giving primary Cl- secretion with Na+ and water following.

   • A: Proton secretion is not the mechanism.
   • B: Chloride, not bicarbonate, secretion drives the diarrhoea.
   • C: cAMP is increased, not decreased.
   • D: Cl- secretion is increased, not decreased.

   Full explanation

   Cholera toxin activates adenylate cyclase and increases cyclic adenosine monophosphate (CAMP). CAMP activates the Cl-secretory channels and produces a primary secretion of Cl- with Na+ and H20.

3. Question 3 · Absorption of Vitamins in Small Intestine

   A man aged 25 attends the ED with abdominal pain. He has a history of Crohn's disease and has had a previous resection of his terminal ileum.

   Which of the following is most likely to be deficient because the terminal ileum is absent?

   1. AVitamin C
   2. BVitamin D
   3. CDietary protein
   4. DZinc
   5. EDietary carbohydrate
   Show answer and explanation

   Answer: B. Vitamin D (and B12) are absorbed maximally in the terminal ileum, so resection causes deficiency.

   • A: Not a recognised terminal ileum absorption site; B12 and vitamin D are.
   • C: Protein is absorbed mainly in the proximal small bowel.
   • D: Absorbed mainly in the proximal small bowel.
   • E: Carbohydrate is absorbed mainly in the duodenum and jejunum.

   Full explanation: Absorption of Vitamins in Small Intestine

   Vitamins absorption  

   • Fat soluble vitamins (A, D, E, and K) are incorporated into micelles and absorb along with other lipids.
   • Most water-soluble vitamins are absorbed by Na+ -dependent cotransport mechanisms.
   • Vitamin B12 is absorbed in the ileum and requires intrinsic factors.
   • The vitamin B12-intrinsic factor complex binds to a receptor on the ileal cells and is absorbed.  
   • Gastrectomy results in loss of parietal cells, which are source of intrinsic factor. Injection of vitamin B12 required to prevent pernicious anemia
   •  Ileectomy results in loss of absorption of vitamin B12-intrinsic factor complex and thus requires injection of vitamin B12 

4. Question 4 · Innervation of Gi Tract

   A Baby defecates after eating because of which one of the following physiological reflex?

   1. AEntero-colic reflex
   2. BOesophageo-gastric reflex
   3. CVagal reflex
   4. DOesophageo-colic reflex
   5. EGastro-colic reflex
   Show answer and explanation

   Answer: E. The gastrocolic reflex increases colonic motility in response to gastric stretch after a meal.

   • A: Not the named reflex triggered by gastric stretch.
   • B: Relates to the upper gut, not colonic motility.
   • C: Non-specific term; gastrocolic names this response.
   • D: Not the named reflex for post-meal colonic motility.

   Full explanation

   The gastrocolic reflex is a physiological reflex that controls the motility of the lower gastrointestinal tract following a meal. As a result of the gastrocolic reflex, the colon has increased motility in response to the stretch of the stomach with the ingestion of food.

5. Question 5 · Gastrointestinal Hormones

   You prescribed a proton pump inhibitor to a patient with duodenal ulcer. Regarding the pathophysiology of peptic ulcer disease, which one of the following statements is correct?

   1. AThick gastric mucosa formation
   2. BDecrease prostaglandin synthesis
   3. CIncreased prostaglandin synthesis
   4. DDecrease gastrin secretion
   5. EDecreased Hcl secretion from gastric parietal cells
   Show answer and explanation

   Answer: B. Prostaglandins inhibit gastric secretion and stimulate bicarbonate secretion, so reduced synthesis (as with NSAIDs) predisposes to peptic ulcer disease.

   • A: Mucosal protection is reduced, not enhanced by thickened mucosa.
   • C: Increased prostaglandins are protective, not causative.
   • D: Reduced gastrin is not the mechanism; loss of prostaglandin protection is.
   • E: Prostaglandins inhibit acid, so losing them raises, not lowers, acid secretion.

   Full explanation: Gastrointestinal Hormones

   Gastrointestinal hormones

   GI Hormone are released from endocrine cells in the GI mucosa into portal circulation, enter the general circulation, and have physiologic actions on target cells. 

   Gastrin  

   Gastrin hormone is released from G-cells in the lining pyloric antrum of stomach.  

    Stimulating factors 

   Gastrin secretion is stimulated by: 

   • The presence of small peptides and amino acids in chyme
   • Gastric distension
   • Vagal stimulation directly via acetylcholine and indirectly via gastrin releasing peptide (GRP)
   • Raised gastric PH (H+)

   Inhibiting factors  

   Gastrin secretion is inhibited by. 

   • Low gastric PH by negative feedback mechanism
   • Somatostatin
   • Secretin 
   • Gastric inhibitory polypeptide (GIP)
   • Cholecystokinin

   Action of Gastrin 

   • Stimulate the acid secretion from gastric parietal cells (both by directly and indirectly by stimulating release of histamine from ECL cells
   • Stimulate pepsinogen secretion from chief cells.
   • Stimulate growth of gastric mucosa by stimulating the synthesis of RNA and new protein

    

   Zollinger-Ellison syndrome (Gastrinoma) 

   •  Occurs when gastrin is secreted by non-β-cell tumors of the pancreas. 

    Secretin  

   • Secretin is released by S-cells in the duodenum. 

   Stimulating factors  

   Secretin secretion is stimulated by: 

   • A low PH (H+) in the duodenum
   • The presence of products of fat digestion in the duodenum

   Inhibitory factors  

   • Secretin release is inhibited by somatostatin. 

   Action of secretin  

   Secretin acts to: 

   • Decrease gastric acid secretion by gastric parietal cells (through inhibition of gastrin release)
   • Inhibit the gastric emptying. 
   • Stimulate the release of pepsinogen by gastric chief cells.
   • Stimulate the pancreatic HCO3- secretion. 
   • Potentiate cholecystokinin-induced stimulation of pancreatic enzyme secretion.
   • Stimulate HCO3- and H2O secretion by the liver and increase bile production.

    Cholecystokinin (CCK) 

   •  CCK is released from I cells of the duodenal and jejunal mucosa. 

   Stimulating factors  

   Cholecystokinin release is stimulated by: 

   • The presence of small peptides and amino acids in the duodenum
   • The presence of fatty acids and monoglycerides in the duodenum
   • Triglycerides do not stimulate the release of CCK because they cannot cross intestinal cell membranes. 

   Inhibiting factors  

   The release of cholecystokinin is inhibited by somatostatin. 

   Action of CCK 

   • Stimulate the pancreatic enzyme secretion. 
   • Stimulate the secretion of pepsinogen from chief cells.
   • Stimulate the contraction of gall bladder and simultaneously cause relaxation of the sphincter of Oddi for secretion of bile.
   • Potentiates secretin-induced stimulation of pancreatic HCO3- secretion.
   • Inhibit the Gastric acid production. 
   • Inhibit the gastric emptying, thus meals containing fat stimulate the secretion of CCK, which slow gastric emptying to allow more time for intestinal digestion and absorption.   

    

    Overview of GIT hormones

   Hormones	Site of secretion	Stimulating factor	Inhibiting factors	Action
   Gastrin	G-cells in the pyloric antrum	The presence of small peptide and amino acids in the stomach gastric distension raised gastric PH vagal stimulation	Low gastric PH Somatostatin Secretin Cholecystokinin gastric inhibitory polypeptide	Stimulate acid secretion from gastric parietal cells, stimulate pepsinogen from gastric chief cells, increase gastric motility, stimulate growth of gastric mucosa
   Secretin	S-cells in the duodenum	A low PH and the presence of fatty acids in the duodenum	Somatostatin	Inhibit gastric acid secretion. Inhibit gastric emptying. Stimulate pepsinogen secretion. Stimulate pancreatic bicarbonate secretion. Increase pancreatic enzyme secretion. Increase bile production.
   Cholecystokinin (CCK)	I-cells in the duodenum and jejunum	The presence of fatty acids/ monoglycerides and small peptides/amino acids in the duodenum	Somatostatin	Increase production of bile Stimulate release of stored bile Increase pancreatic bicarbonate secretion. Stimulate pancreatic enzyme secretion. Inhibit gastric emptying. Inhibit gastric acid production. Stimulate pepsinogen secretion.
   Gastric inhibitory polypeptide	K-cells in the duodenum and jejunum	The presence of fatty acids, amino acids and orally administered glucose in the duodenum	Somatostatin	Inhibit gastric acid secretion. Stimulate the insulin release.

   Somatostatin 

   • In the gut, somatostatin is secreted from the D-cells in the gastric and intestinal mucosa. Somatostatin inhibits the release of all GI Hormones. 
   • In the pancreas, somatostatin is produced by delta cells of islets of Langerhans.
   • Somatostatin is secreted by cells throughout the GI tract in response to H+ in the lumen.
   • Due to its effect on growth hormone, it is also referred to as growth hormone inhibiting hormone. 
   • Somatostatin secretion is inhibited by vagal stimulation.
   • Somatostatin inhibits the gastric acid secretion both directly at the parietal cell via a G-protein coupled receptor and indirectly via inhibition gastrin and histamine secretion.

   Action of somatostatin 

   • Inhibit the release of all GI hormone (gastrin, secretin, CCK, GIP, insulin glucagon) 
   • Decrease gastrin release leading to reduced gastric acid.
   • Decrease gastric and intestinal secretions.
   • Decrease bile production and release.
   • Decrease pancreatic exocrine and endocrine function. 
   • Paracrine inhibition of insulin and glucagon secretion from α and β-cells of the Islets of Langerhans
   • Decrease blood glucose concentration.